This research is intended to provide information on the neurochemical mechanisms which mediate the retrieval of temporarily inaccessible memories. Recent research has shown that learned behaviors apparently forgotten following amnesic agents like electro-convulsive shock or drug treatments, or weakened by the passage of time can be made accessible by presentation of reminder cues, neuropeptides or catecholamine agonists before the memory test. These studies focus attention on the important role of retrieval failure in the etiology of forgetting. In additon they show that the stimulation of retrieval processes is a powerful tool for alleviating forgetting. Little is known about the physiological processes which mediate facilitated retrieval. Pharmacological data from our laboratory indicate that the CA neurotransmitter systems may play a central role in mediating retrieval of inaccessible memories. The present research is a test of this idea. In these experiments forgetting is induced for several types of learned behaviors by different treatments. These include conventional amnestic agents (ECS, anoxia and protein synthesis inhibition), the imposition of long delays between training and testing and the use of memory deficient senescent animals. Pharmacological agents which activate CA systems (releasing agents and receptor agonists and antagonists) are introduced prior to testing to determine whether these treatments will alleviate forgetting. Experiments will test the generality of the CA hypothesis across different forgetting treatments and learning tasks, evaluate the relative contribution of central and peripheral CA systems, assess the roles of norepinephrine and dopamine and their interactions with non-CA systems and investigate the strength and durability of the pharmacologically reactivated memory. These experiments should increase our understanding of the mechanisms underlying retrieval of memory from storage and may also provide clues for the development of drug therapies to alleviate memory disorders in man resulting from senescence, brain injury and stroke.